Heat Shock Protein 60 as an Immunomodulator in Heart Diseases

Cardiac muscle cells are specialised rod-shaped cells with a single nucleus that are connected to each other by intercalated discs. They are extremely important for the functioning of the heart, as they are responsible for the propagation and effectiveness of contraction. Mitochondria within these cells are vital for adenosine triphosphate (ATP) synthesis, redox balance, calcium homeostasis, and lipid synthesis. Heat shock protein 60 (Hsp60), a mitochondrial chaperonin, plays a crucial role in protein folding. The expression of Hsp60 increases when the heart is under stress, such as during a heart attack or heart failure. Hsp60 is located not only inside the cell, but has also been localised in small and large vesicles, in the cell membrane and freely in the cell culture medium or in the blood. And it is precisely in the latter form that this chaperonin could play a decisive role as an immunomodulator. In this review, we have brought together various studies to discuss and highlight the distribution of Hsp60 in cells, its association with apoptosis and its action as a damage-associated molecular pattern (DAMP) that interacts with Toll-like receptors to modulate immune responses. The link to heart disease arises from a connection to heart-specific microRNAs whose expression can be affected by dysregulation of Hsp60. In summary, we hypothesise that Hsp60 may also have an immunomodulatory effect under stress conditions.